Ovarian carcinoma remains one of the most lethal gynecologic malignancies. It has been reported to be the fifth most common cancer and the fourth leading cause of cancer mortality among women in the United States (see Maller et al., SEER Cancer Statistics Review. 1973–1990, Bethesda, Md., National Cancer Institute(1993)).
Due to the lack of powerful diagnostic tests and also to the absence of any overt symptoms, early detection of ovarian cancer is difficult. In approximately two-thirds of patients, the disease is at an advanced stage (i.e., stage III or IV) at the time of diagnosis (see Boring et al., Ca. Cancer J. Clin. 44:7–26 (1994); Coppleson et al., Gynecologic Oncology: Fundamental Principles and Clinical Practice, 2nd ed, London, Churchill Livingstone Press (1992); Hung et al., “The Female Reproductive System: Cell Lines from Tumor of the Human Ovary and Uterus”, in Hay et al., Atlas of Human Tumor Cell Lines, Academic Press, San Diego, pp 359–386(1994)). Currently, diagnostic assays are limited to a few markers. Numerous studies on ovarian carcinomas have reported genetic alterations in oncogenes and tumor suppressor genes (see, e.g., Piver et al., Semin. Oncol. 18: 177–85 (1991)). Specifically, amplification or activation of the oncogenes HER-2/neu, K-ras and c-myc, as well as inactivation of the tumor suppressor genes p53, BRCA1 and the human mismatch repair genes hMLH1, hMSH2, hPMS1 and hPMS2, have been detected in ovarian cancers. It has been reported that mutation of the p53 gene occurs in about 30–50% of ovarian cancers (see, e.g., Berchuck et al., Am. J. Obstet. Gynecol. 170:246–52 (1994)). p53 gene mutations are common in a variety of other tumors, however.
Accordingly, there exists a need to identify new markers associated with ovarian cancer and other epithelial cancers. The present invention satisfies this and other needs.